dr. Shirley L A, Sp.

A
23 November 2011

SHOCK
An acute dramatic syndrome
Characterized by inadequate circulatory
provision of oxygen


Metabolic demands of vital organs
and tissues are not met

SHOCK
Insufficient O2 is delivered to
support aerobic cellular
metabolism
There is a shift to less efficient
anaerobic metabolism
Leads to lactic acidosis
If inadequate tissue perfusion continues
Various endocrine,
vascular, inflammatory,
metabolic, cellular &
systemic responses occur
Patient becomes more
physiologically
unstable
Shock is a progressive process
Intially may be compensated
But then may progress to
uncompensated condition
Untreated shock will lead to
irreversible tissue injury & death
Epidemiology
Shock occurs in approximately
2% of all hospitalized children &
adults in US
Mortality rate is 20 - 50%
Multiple organ dysfunction
increases the probability of death
1 organ system involved 25%
2 - 60%
3 or > - 85%
There are 5 major types of
shock:
hypovolemic, septic,
cardiogenic, distributive, and
obstructive

Hypovolemic (diarrhea-
dehydration, hemorrhage)
and septic shock are the
most common causes of
shock in children
Clinical classification of shock
Type of
Shock
Septic Cardiogenic Distributive
Characteristics
Infectious organisms
release toxins that
affect fluid distribution,
cardiac output & so on
Primary pump
failure produces
inadequate tissue
perfusion;resultant
metabolic acidosis
further impairs
cardiac function
Neurologic
disturbance may
cause uneven
distribution of fluids,
leading to acidosis
Overdose of drug can
alter fluid distribution

Sample
causes
Bacterial
Viral
Fungal
(all are more likely in
immunocompromised)
Ischemic insult
Cardiomyopathy
CHD
Neurogenic
(disturbance of
vasomotor tone)
Anaphylaxis
Toxins
Allergic reactions
Clinical classification of shock
Type of Shock Hypovolemic Obstructive
Characteristics
Reduced fluid volume
Reduces cardiac output;
metabolic acidosis can result
from low intravascular
volume and poor tissue
perfusion; serious electrolyte
abnormalities may occur
Poor cardiac output,
cyanosis, hypotension,
narrow pulse pressure

Sample causes Enteritis
Hemorrhage
Extensive burns
Diabetes insipidus
Adrenal insufficiency
Tension pneumothorax,
pericardial tamponade
Pathophysiology
An initial insult triggers shock thus disrupting blood
flow to end-organs leading to inadequate tissue
perfusion
The body's compensatory mechanisms are initiated to
maintain perfusion to vital organs, leading to
compensated shock
If treatment is not introduced during this period of
compensated shock, decompensated shock develops,
causing tissue damage that leads to multisystem organ
dysfunction and death
Algorithm for
decompensated shock
Initial insult
Triggers shock
Decreased perfusion
Bodys compensatory mechanisms
Compensated
shock
Decompensated shock
Tissue damage
Multiple organ failure
Death
In early phases of shock, a number of compensatory
physiologic mechanisms act to maintain BP and preserve
tissue perfusion

increase HR, stroke volume & vascular smooth muscle tone,
regulated through neurohormonal changes in sympathetic
nervous system activation and other hormonal responses to
help preserve blood flow to vital organs such as brain, heart,
and kidneys
RR to promote the excretion of CO
2
to compensate for
increased CO
2
production and the metabolic acidosis that
occurs due to poor tissue perfusion. Increased renal
excretion of hydrogen ions and retention of bicarbonate
occurs in an effort to maintain normal pH

Maintenance of vascular volume is facilitated by the renin-
angiotensin-aldosterone & atrial natriuretic factor axes
(through regulation of sodium), cortisol & catecholamine
synthesis and release, and secretion of ADH

Despite these compensatory mechanisms, intravascular
fluid leaks into the interstitial extracellular space because of
vascular endothelial cell injury and loss of tight junctions

Pathophysiology of Shock
EXTRACORPOREAL FLUID LOSS Hypovolemic shock may be
due to direct blood loss through hemorrhage or abnormal loss of
body fluids (diarrhea, vomiting, burns, diabetes mellitus or insipidus,
nephrosis)

LOWERING PLASMA ONCOTIC FORCES Hypovolemic shock
may also result from hypoproteinemia (liver injury, or as a
progressive complication of increased capillary permeability)

ABNORMAL VASODILATION Distributive shock (neurogenic,
anaphylaxis, or septic shock) occurs when there is loss of vascular
tone venous, arterial, or both (sympathetic blockade, local
substances affecting permeability, acidosis, drug effects, spinal cord
transection)
Pathophysiology of Shock
INCREASED VASCULAR PERMEABILITY Sepsis may change the
capillary permeability in the absence of any change in capillary
hydrostatic pressure (endotoxins from sepsis, excess histamine
release in anaphylaxis)

CARDIAC DYSFUNCTION Peripheral hypoperfusion may result
from any condition that affects the heart's ability to pump blood
efficiently (ischemia, acidosis, drugs, constrictive pericarditis,
pancreatitis, sepsis)
Sepsis, pancreatitis, and SIRS can produce direct myocardial
depressant effects adding a cardiogenic component to patients with
septic shock
All forms of shock affect heart rate
poor tissue perfusion
afterload
preload
myocardial
contractility
Fluid loss
(vomiting,
diarrhea,
hemorrhagic
trauma,severe
burns)
initial in
vascular
resistance
maintain BP
& restore
circulating
intravascular
volume
hypotension
develops &
produces tissue
ischemia
Significant electrolyte
alterations
pre-existing low
plasma oncotic
pressure (nephrotic
syndrome,
malnutrition, hepatic
dysfunction, acute
severe burns)
greater
capillary
leaking
intravascular
volume,more
edema,
potentially
worsens the
respiratory
status
SHOCK
Distributive shock

Abnormal vasodilation results in
vasodilatory shock and is usually
caused by sepsis, hypoxia, poisonings
(carbon monoxide, cyanide,
metformin), anaphylaxis, neurogenic
events, or mitochondrial dysfunction

The lower systemic vascular resistance
(SVR) is usually accompanied by an
increase in cardiac output and a
redistribution of blood flow away from
vital organs to nonvital organs; hence,
the term distributive shock
shock occurs only with low
BP (hypotension)

Through various compensatory
mechanisms, hypotension is often
a late finding

Hypotension is an advanced state
of decompensated shock and has
a high mortality rate
Tachycardia, with or without
tachypnea, may be the 1st or
only sign of early compensated
shock
Shock may be present with normal BP if other factors do
not permit the patient to maintain adequate tissue oxygen
delivery
Anemia and hypoxia result in reduced oxygen delivery at
any given cardiac output
Fever and trauma may increase tissue oxygen and
metabolic requirements
Progression of any of the mechanisms that lead to shock
results in hypoxia and lactic acidosis

Conversely, if blood pressure is low, but tissue perfusion is
adequate to meet the metabolic demands of the body,
shock may not be present



vital signs
physical examination findings
laboratory studies
presence or absence of acidosis

to determine if the pediatric patient
is in shock

CLINICAL MANIFESTATIONS
ORGAN SYSTEM PERFUSION PERFUSION PERFUSION
Central nervous system Restless, apathetic,
anxious
Agitated/confused,
stuporous, coma
Respiration Ventilation Ventilation
Metabolism Compensated metabolic
acidemia
Uncompensated
metabolic acidemia
Gut Motility Ileus
Kidney Urine volume Oliguria (<0.5 mL/kg/hr) Oliguria/anuria
Urinary specific gravity
Skin Delayed capillary refill Cool extremities Mottled, cyanotic, cold
extremities
Cardiovascular system Heart rate Heart rate Heart rate, blood
pressure, central pulses
only
Hypovolemic shock
usually presents as changes in mental status,
tachypnea, tachycardia, hypotension, poor peripheral
pulses, cool extremities, and oliguria
Supine hypotension and tachycardia are hallmarks of
hypovolemia
Neonates and infants may also have poor urine output.
Dry mucous membranes, dry axillae, and poor skin
turgor are variably present
Hypovolemic shock may initially present with normal or
only slightly cool distal extremities
Septic shock
has 2 phases:
1. Early, or warm, shock is diagnosed by low SVR
2. late, or cold, shock is diagnosed by high SVR

Septic shock may present initially with :
- warm extremities (from peripheral vasodilation
secondary to low SVR)
- bounding pulses (from high stroke volume and widened
pulse pressure)
- tachycardia
- tachypnea
- adequate urination
- mild metabolic acidosis
Cardiogenic shock
cool extremities
delayed (>23 sec) capillary filling time
hypotension
poor peripheral or central pulses
tachypnea
increasing obtundation
decreased urination

all caused by peripheral vasoconstriction & decreased CO
Uncompensated shock (high vascular resistance,
decreased CO, obtundation, oliguria) occurs late in the
progression of shock, regardless of its etiology




Compensated shock
decompensated
shock
h
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- in lactic acid production
- very low mixed venous 02 sat
indicating inadequate oxygen
delivery
Measurement of the oxygen saturation of
central mixed venous blood (Mvo
2
)
- from the PA, RV, RA, SVC, or IVC can determine if
overall peripheral oxygen delivery (the true standard for
such measurements is the pulmonary artery) is adequate
- Mvo
2
should be 2025% < the arterial 02 sat (N Mvo
2
is
7580%)
- A low Mvo
2
suggests poor perfusion
- This can guide caregivers in the use of fluid support and
inotropic agents to improve cardiac output in the
treatment of shock

Treatment
Initial management :
ABCs of resuscitation
(airway, breathing, & circulation)

Neonates and infants in particular may
also have profound hypoglycemia
associated with shock; it maybe helpful
to recognize the ABCDs, with the D
standing for dextrose in the pediatric
population
In most patients with early shock

fluid bolus of 20 mL/kg of normal
saline or lactated Ringer solution in
510 min
If it is not possible to insert an
intravenous catheter into a peripheral
vein within 90 sec or within 3
attempts, an intraosseous infusion
reassessed !!! more fluid ?
Antibiotics? vasoactive agents?
Colloids?
Cardiogenic shock ?
the fluid bolus should be held or a smaller
volume given over a longer period to avoid
exacerbating heart failure
Children in severe hypovolemic,
septic, or anaphylactic shock may
require additional fluid boluses
(6080 mL/kg within the 1st 12 hr of
presentation)
Fluid therapy should be titrated until improvements are
noted
Heart rate
Blood pressure
Urine output
level of
consciousness
capillary refill time
Cardiovascular Drug Treatment of Shock
DRUG EFFECT(S) DOSE RANGE COMMENTS
Dopamine Strengthens contractions
(throughout dose range)
Intermediate dose =
515 g/kg/min

increasing risk of dysrhythmias at high dose
increases renal blood flow
(low/intermediate doses)
High dose = 1525
g/kg/min

Should be administered in a central vein

Vasoconstriction (high doses)
Epinephrine Increases heart rate and
strength of contractions
0.053.0 g/kg/min May lessen renal perfusion
Potent vasoconstrictor Causes high O
2
consumption in the heart
High risk of dysrhythmia
Dobutamine Increases strength of heart
contraction
120 g/kg/min Very weak vasoconstriction (high dose)
Little effect on heart rate Good for cardiogenic shock; strengthens heart contraction
and produces afterload reduction
Peripheral vasodilator,
especially in vessels to
viscera

Cardiovascular Drug Treatment of Shock
DRUG EFFECT(S) DOSE RANGE COMMENTS
Norepinephrine Strong vasoconstrictor 0.051.5 g/kg/min Produces short-term rise in
blood pressure (high systemic
vascular resistance)
Weak effect on strength
of heart contraction
Causes increase in O
2

consumption, tendency for
dysrhythmias
Phenylephrine Strong vasoconstrictor 0.52.0 g/kg/min Can cause sudden
hypertension
Can be used to slow
tachycardia through
reflex cardiac slowing
Causes increase in O
2

consumption
Milrinone Potent inotrope Load 50 g/kg over
15 min
Phosphodiesterase inhibitor
slows cyclic adenosine
monophosphate breakdown
Potent chronotrope 0.51 g/kg/min
Peripheral vasodilator